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|標題:||Glycyrrhizic Acid and 18 beta-Glycyrrhetinic Acid Modulate Lipopolysaccharide-Induced Inflammatory Response by Suppression of NF-kappa B through PI3K p110 delta and p110 gamma Inhibitions||作者:||Wang, Chung-Yi
|關鍵字:||glycyrrhizic acid;18 beta-glycyrrhetinic acid;anti-inflammatory;lipopolysaccharide;macrophage;mouse macrophage cells;nitric-oxide synthase;antiinflammatory;activity;raw-264.7 macrophages;bioactive compounds;murine;macrophages;cox-2 expression;natural-prod||Project:||Journal of Agricultural and Food Chemistry, Volume 59, Issue 14, Page(s) 7726-7733.||摘要:||
The roots and rhizomes of licorice (Glycyrrhia) species have been used extensively as natural sweeteners and herbal medicines. The aim of this work was to determine the in vitro anti-inflammatory effects of glyc-yrrhizic acid (GA) and 18 beta-glycyrrhetinic acid (18 beta GA) from licorice in a lipopolysaccharide (LPS)-stimulated macrophage model. The results showed that treatment with 25-75 mu M GA or 18 beta GA did not reduce RAW 264.7 cell viability but did significantly inhibit the production of LPS-induced nitric oxide (NO), prostaglandin E(2) (PGE(2)), and intracellular reactive oxygen species (ROS). Western blotting and reverse transcriptase polymerase chain reaction (RT-PCR) analyses revealed that GA and 18 beta GA significantly reduced the protein and mRNA levels of iNOS and COX-2 in LPS-induced macrophages. Both GA and 18 beta GA inhibited the activation of NF-kappa B and the activities of phosphoinositide-3-kinase (PI3K) p110 delta and p110 gamma isoforms and then reduced the production of LPS-induced tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, and IL-1 beta in a dose-dependent manner. In conclusion, these results indicate that GA and 18 beta GA may provide an anti-inflammatory effect by attenuating the generation of excessive NO, PGE(2), and ROS and by suppressing the expression of pro-inflammatory genes through the inhibition of NF-kappa B and PI3K activity. Thus, the results suggest that GA and 18 beta GA might serve as potential agents for the treatment of inflammatory-mediated diseases.
|Appears in Collections:||食品暨應用生物科技學系|
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